Cadoo v BHP Billiton Limited
[2012] SADC 31
•16 March 2012
District Court of South Australia
(Civil)
CADOO v BHP BILLITON LIMITED
[2012] SADC 31
Judgment of His Honour Judge Lovell
16 March 2012
TORTS - NEGLIGENCE - ESSENTIALS OF ACTION FOR NEGLIGENCE - DUTY OF CARE - REASONABLE FORESEEABILITY OF DAMAGE
The plaintiff was employed by the defendant in the shipyard in Whyalla from 1961 to 1964 when he was exposed to asbestos dust from products being used in ship construction. Defendant's knowledge of the risks of exposure to asbestos dust. Extent of information on "risk" in the public domain. Whether risk "reasonably foreseeable". Whether defendant breached duty of care.
Held: Risk of dust disease reasonably foreseeable. Defendant breached duty of care.
Dust Diseases Act 2005 (SA) s 8, referred to.
Parker v BHP Billiton Limited [2011] SADC 104, applied.
Wyong SC v Shirt (1980) 146 CLR 40; Cole v South Tweed Heads Rugby League Football Club and another (2004) 217 CLR 469; Neindorf v Junkovic (2005) 80 ALJR 341; Mt Isa Mines v Pusey (1970) 125 CLR 383; Amaca Pty Ltd v Hannell (2007) 34 WAR 109; Mulligan v Coffs Harbour City Council (2005) 223 CLR 486, per Hayne J at 501; Vairy v Wyong Shire Council (2005) 223 CLR 422, per Hayne J at 462; Mulligan v Coffs Harbour City Council (2005) 223 CLR 486, per Gleeson CJ and Kirby J at 491; Thompson v Woolworths (Q'land) Pty Ltd (2005) 79 ALJR 904 at 911; Graham Barclay Oysters Pty Ltd v Ryan (2002) 211 CLR 540; Roman Catholic Church Trustees for the Diocese of Canberra v Hadba (2005) 221 CLR 161, discussed.
DAMAGES - MEASURE AND REMOTENESS OF DAMAGES IN ACTIONS FOR TORT - MEASURE OF DAMAGES
Plaintiff suffers from asbestosis and asbestos related pleural disease. Damages Assessed.
CADOO v BHP BILLITON LIMITED
[2012] SADC 31Background
Mr Cadoo was employed by the defendant at its Whyalla Shipyards from 1961 to 1964. During that time he alleges that he was exposed to asbestos. He alleges that his exposure at the Whyalla Shipyards contributed to his asbestos related conditions he subsequently contracted. He had been exposed to asbestos whilst working in shipyards in Northern Ireland.
The defendant denied that Mr Cadoo suffered from any asbestos related disease and further, even if he did, it had not acted negligently in its use of asbestos related products.
Mr Cadoo died in April 2003 from a heart condition unrelated to his exposure to asbestos.
Mr Cadoo’s claim was run concurrently with Mr Parker’s (by order of a Master of this Court). Both parties urged the learned Master to make the order.
The judgment in Mr Parker’s matter was delivered on 18 July 2011. Given the two matters ran concurrently, the delivery of a later judgment here requires an explanation.
The writing of the liability component of Mr Parker’s judgment (for reasons discussed in that judgment) was time consuming. Mr Cadoo died in April 2003 and damages, even on the plaintiff’s best case, were going to be extremely modest. Mr Cadoo’s action was for all practical purposes, a determination of liability. For those reasons other work commitments took priority.
The parties accepted that, other than the medical evidence relating to each party, the general evidence was admissible in relation to both actions. There were some exceptions to this and I deal with them in these reasons.
Parts of this judgment are simply a repetition of findings made in Mr Parker’s matter. I do not intend to include the discussion of all of the evidence from Mr Parker’s matter.
In these reasons I deal with the evidence that related specifically to Mr Cadoo’s matter. I adopt those findings set out in the Parker judgment that relate to the general background, the scientific and medical articles, the general working conditions at the “fit-out” wharf, Dr Becklake’s evidence and my findings in relation to the NH&MRC documents. I also adopt my findings in relation to the “Wilson Report” although the report is of limited relevance given the time when Mr Cadoo stopped working for the defendant.
Liability
Mr Cadoo died on 18 April 2003 from a heart condition. On 17 June 2002, for the purposes of his claim in the Dust Diseases Tribunal (NSW) (as it then stood) Mr Cadoo swore and filed an affidavit outlining his exposure, as he believed it, to asbestos during his working life. His affidavit was tendered.[1]
[1] Exhibit PC5.
I referred to his affidavit in my judgment in Mr Parker’s matter.[2] I repeat the relevant parts.
[2] Parker v BHP Billiton Limited [2011] SADC 104 at [159]-[165].
Mr Cadoo was born in 1923 in Northern Ireland. He became a boilermaker working on ships at a firm called Harland & Wolff Limited in Northern Ireland. He spent a significant amount of time installing the boilers into ships. Asbestos lagging was applied to pipes and other steam vessels on the ships.
With his wife, Mr Cadoo migrated to Australia in 1960. He worked at the Whyalla Shipyards from 1961 to 1964. Mr Cadoo could recall working on the PJ Adams, the Seaway King and the Seaway Queen amongst other ships.
Mr Cadoo said he was not exposed to much asbestos while working at Whyalla as almost all of his work was done on board the ships before they were launched. He did work on the PJ Adams after it was launched and he was exposed to asbestos dust and fibre.
While he did not see asbestos being sprayed, he could recall asbestos blocks, pipe sections and rope being cut and fitted to size. Dust was released at that time.
Small pieces of insulation would fall to the ground and remain there until cleaned up. When kicked or touched the asbestos released dust.
He would occasionally use asbestos gloves when welding.
Mr Cadoo was not warned at Whyalla (or at any of his work places) about the dangers of working with asbestos. He was not required to wear a mask or take any other precaution to avoid the inhalation of asbestos dust and fibre.
Mr Cadoo’s work records establish he worked at the defendant’s shipyards from 3 July 1961 to 17 February 1964.[3]
[3] Exhibit PC15.
I find that Mr Cadoo worked on the PJ Adams after it was launched and had been sent to the “fit-out” wharf. This was not in dispute.
Exactly how long Mr Cadoo was exposed to asbestos on the PJ Adams is not entirely clear. Mr Ewbank gave evidence about the Iron Hunter where he was dismissive of the suggestion that the lagging work could have been done in seven weeks. The records indicate that, in terms of size, the PJ Adams and the Iron Hunter were similar (albeit different types of ships). They were both bigger than many of the ships constructed at the shipyards.
Mr Dennis, who worked on the PJ Adams, said the laggers generally could be there for months.
I cannot be precise. I find that Mr Cadoo worked on the PJ Adams while lagging work was being undertaken for at least a couple of months, probably longer. The PJ Adams was launched on 10 January 1962 and completed by 29 October 1962.[4] His greatest exposure must have been during that period.
[4] Exhibit D8.
I do not accept the defendant’s submission that his exposure would not have exceeded a “few months” and that it was minimal.
The failure of Mr Cadoo to mention his exposure to asbestos to Dr Chapman remains unexplained. Clearly he was exposed. His failure to mention this matter to Dr Chapman does not make me doubt his statements in the affidavit.
As mentioned, I adopt the findings made in the Parker judgment relating to the working conditions at the “fit-out” wharf. I do not intend to repeat the evidence or the findings.
Mr Cadoo finished working at Whyalla in February 1964. While some of the witnesses in Mr Parker’s case gave evidence of conditions post 1964, I find that the method of operation adopted by the defendant at the “fit-out” wharf did not change in anything other than a minor way throughout the periods discussed by the witnesses.[5]
[5] Parker v BHP Billiton Limited [2011] SADC 104 at [156].
A number of the witnesses were working around the same time as Mr Cadoo; that is also true of witnesses whose affidavits were tendered.
Findings
I find that Mr Cadoo was exposed to asbestos whilst working on the PJ Adams at the “fit-out” wharf. Consistent with my findings in Mr Parker’s judgment I find:
·Limpet asbestos was sprayed on the ships although this was sprayed at night. Asbestos lagging was installed on the ships at the “fit-out” wharf. Marinite containing asbestos was used on the ships. This procedure was adopted on the PJ Adams.
·In order to install the “lagging” asbestos pipe sections were cut in the hold of the ships creating dust. Marinite sheets were also cut on board the ships creating dust. The asbestos slurry used in relation to the lagging was sometimes mixed on the wharf but also regularly mixed on board the ships. This was a dusty process. Asbestos rope was also used on the ships. Lagging of pipes and other areas occurred for most of the time a ship was at the “fit-out” wharf. Tasks were performed by other workers on scaffolding.
·Asbestos mattresses were used on board the ships and also, to some extent, made on board the ships. The evidence does not allow me to find that this was other than an occasional activity. I ignore the evidence of “mattresses” when coming to my conclusions.
·Leaving aside the spraying at night of limpet asbestos, asbestos dust and fibre was released into the atmosphere as a result of the other processes mentioned. This occurred while people, such as Mr Cadoo, were working alongside those trades or at least nearby.
·The spraying of limpet asbestos at night left overspray of asbestos on the floor. This was present while people were working in those areas during the day. While the “painters and dockers” were employed to keep the areas clean, other trades would, from time to time, clean the areas in which they were working.
·The sweeping or clean up of the debris caused asbestos dust and fibre to become airborne. No industrial vacuum cleaners were used. The atmosphere became very dusty.
·No attempt was made to suppress the dust generated by “wetting” it.
·The work conducted at the “fit-out” wharf was performed in a very similar manner for many years. The work carried out up to 1971/72 had not changed to any significant degree since the late 1950s.
·No respirator and/or mask were provided to the plaintiff. He was not warned of the dangers of working in an area where asbestos dust/fibre was being released into the atmosphere.
·No mechanical ventilation was generally operating for the clearing of dust. There may have been occasional mechanical ventilation operating while “welding” operations were occurring.
Mr Cadoo was exposed to all of these potential sources of asbestos while working at the “fit-out” wharf on the PJ Adams.
The Law
As discussed in the Parker judgment, a defendant is liable in negligence only when he owes a duty of care to a plaintiff, breaches that duty and, as a result causes injury to the plaintiff of a kind that was reasonably foreseeable. If the defendant owes the plaintiff a duty of care, breach of that duty is determined by considering whether an act or omission of the defendant gave rise to a risk of injury to the plaintiff that, by the exercise of reasonable care, could have been foreseen and avoided.
The concept of reasonable foreseeability plays different and separate roles at various stages in an action for negligence. However, in this matter it is not necessary to consider those matters as it was conceded that the defendant owed the plaintiff a duty of care.
A breach of a duty of care depends upon two things. First, the fact that a risk of harm would be created or contributed to by the acts or omissions of the defendant must have been reasonably foreseeable. Secondly, the Court’s assessment of the reasonableness or otherwise of the defendant’s response to this risk. This second step is often referred to as the “Shirt calculus”. In Wyong SC v Shirt, Mason J stated:
The perception of the reasonable man’s response calls for a consideration of the magnitude of the risk and the degree of probability of it’s occurrence, along with the expense, difficulty and inconvenience of taking alleviating action and any other conflicting responsibilities the defendant may have. It is only when these matters are balanced out that the tribunal of fact can confidently assert what is the standard of response to be ascribed to the reasonable man placed in the defendant’s position.[6]
[6] (1980) 146 CLR 40 at 47-48.
Reasonable foreseeability is a precondition to a finding of negligence: a person cannot be held liable for failing to take precautions against a risk that was not, in all the circumstances reasonably foreseeable. However, the fact that a person ought to have foreseen a risk does not, of itself, justify a conclusion that the person was negligent in failing to take precautions against it.
The inquiry into reasonable foreseeability of the risk of harm, as it relates to the breach of the standard of care, is wholly factual. A hindsight analysis is to be avoided. The inquiry into the breach of a duty of care, although made after the event, must attempt to identify what response a reasonable person, confronted with a reasonably foreseeable risk of injury, would have made to that risk.[7]
[7] Cole v South Tweed Heads Rugby League Football Club and another (2004) 217 CLR 469; Neindorf v Junkovic (2005) 80 ALJR 341.
Foreseeability does not mean foresight of the particular course of events causing the harm. Nor does it suppose foresight of the particular harm that occurred, but only of some harm of a like kind.[8]
[8] Mt Isa Mines v Pusey (1970) 125 CLR 383.
What is “reasonable” must be assessed by reference to all members, present and future, of the class of which the plaintiff is a member,[9] and by reference to all the relevant risks, ascertained at the time in question.[10]
[9] Amaca Pty Ltd v Hannell (2007) 34 WAR 109.
[10] Mulligan v Coffs Harbour City Council (2005) 223 CLR 486, per Hayne J at 501; Vairy v Wyong Shire Council (2005) 223 CLR 422, per Hayne J at 462.
A failure to eliminate a risk that is reasonably foreseeable does not establish negligence. In some cases the response of a reasonable person to a foreseeable risk may be to do nothing.[11]
[11] Mulligan v Coffs Harbour City Council (2005) 223 CLR 486, per Gleeson CJ and Kirby J at 491; Thompson v Woolworths (Q’land) Pty Ltd (2005) 79 ALJR 904, at 911.
Once it has been determined that the risk in question was foreseeable, the negligence “calculus” provides a framework for deciding what precautions a reasonable person would have taken. The “calculus” has four components:
1The probability that the harm would occur if care was not taken;
2The likely magnitude or seriousness of that harm;
3The burden of taking precautions to avoid the harm in terms of expense, difficulty and inconvenience of taking alleviating action; and
4Any other conflicting responsibilities the defendant may have, including the social utility of the risk creating activity.
The inquiry at the “breach” stage thus involves identifying with some precision what a reasonable person would have done by way of response to the foreseeable risk.[12] It is for the plaintiff to demonstrate that there was something that the defendant could have done which would eliminate or reduce the risk complained of and which was practicable.[13]
[12] Graham Barclay Oysters Pty Ltd v Ryan (2002) 211 CLR 540; Amaca Pty Ltd v Hannell (2007) 34 WAR 109.
[13] Roman Catholic Church Trustees for the Diocese of Canberra v Hadba (2005) 221 CLR 161.
Breach of Duty of Care
As mentioned the inquiry involves, initially, a determination of the issue of whether a risk of harm was created or contributed to by the acts or omissions of the defendant and that such risk was reasonably foreseeable.
Reasonable Foreseeability
As in the Parker matter, it was relevant to this issue for the plaintiff to establish, at the time the plaintiff was exposed to asbestos dust, what the state of scientific/medical knowledge was as to the dangers of asbestos dust generally and also to the class of persons (workers) of which the plaintiff was a member.
The plaintiff attempted to rely on the provisions in s 8 of the Dust Diseases Act to prove its case on the state of scientific knowledge. The defendant took a number of objections to that process. Submissions were made on the applicability of the provisions.
In the Dust Diseases Act 2005, s 8 deals with ‘Evidentiary presumptions and special rules of evidence and procedure’. Relevantly it states:
(3) The following rules apply in a dust disease action:
(a)the Court may admit evidence admitted in an earlier dust disease action against the same defendant (including in a dust disease action brought in a court of the Commonwealth or another State or Territory);
(b)the Court may dispense with proof of any matter that appears to the Court to be not seriously in dispute;
(c)the Court may invite a party to admit facts of a formal nature, or facts that are peripheral to the major issues in dispute, and may, if the party declines to do so, award the costs of proving those facts against the party.
(4) If—
(a)a finding of fact has been made in a dust disease action by a court of this State, the Commonwealth or another State or Territory; and
(b)the finding is, in the Court’s opinion, of relevance to a dust disease action before the court,
the Court may admit the finding into evidence and indicate to the parties that it proposes to make a corresponding finding in the case presently before the Court unless the party who would be adversely affected satisfies the Court that such a finding is inappropriate to the circumstances of the present case.
There was discussion during the course of the case as to the interpretation of those provisions. In particular, sub-s (4) presented difficulties. No doubt the draftsperson of the legislation intended the provisions to be helpful. The defendant took a series of objections as to how the provisions were to be interpreted. There was merit in many (but not all) of the objections.
A difficulty with the provisions, particularly where the Court is not a specialist tribunal, is that to determine the relevance and then the admissibility of various matters, evidence was required to be given. To that extent the provisions (in the circumstances of this case) were not of much assistance to the plaintiff. The objections (and I intend no criticism of the defendant) led to the position that the plaintiff, from a practical point of view, had to prove his case without resorting to the “aids” in the statute. Given the objections taken by the defendant about what findings I could adopt from other cases (on the defendant’s submissions –none) and their objection to articles and evidence from someone such as Dr Becklake (the article being written in 1976), the only way to resolve the issues was to take the evidence and rule on the relevance and admissibility of the evidence.
No doubt much of this evidence has been led before the Dust Diseases Tribunal or in other cases interstate. However, this was the first case in South Australia against this defendant in relation to a matter coming under the Dust Diseases Act 2005 (SA). Mr King’s claim was being litigated around the same time.
I have approached this judgment on the basis that findings I make may be relevant to those statutory provisions and the way they may be used in future cases. Therefore I considered it important to set out, as far as possible, that material to which I have had regard.
Mr Little SC (and Ms O’Connor) tendered and took me through a large volume of scientific/medical material and I was invited to read it and make a determination as to the state of knowledge at various times of the “dangers” of exposure to asbestos fibre, without the benefit of any expert evidence. In addition, and as an alternative, Mr Little SC also called evidence from Dr Becklake, an epidemiologist. She had written an article which (amongst other matters) contained her opinion on this topic. Objection was taken to her evidence and I dealt with that matter in the Parker judgment.
The defendant also tendered materials related to this issue. I have incorporated that material.
Scientific/Medical Evidence
During the course of the hearing, the plaintiff tendered a large number of scientific, medical and industrial papers and articles relating to the dangers of the use of asbestos in the work place.
I adopt my discussion and findings in relation to those matters as set out in the Parker judgment. That includes my discussion and findings in relation to the evidence of Dr Becklake and the report and relevance of the report of Dr Wilson. It also includes my findings in relation to the evidence of the librarian Ms Batt.
In Mr Cadoo’s matter the relevant “cut off” point regarding knowledge is no later than when he stopped working for the defendant. Indeed, practically speaking, I accept that it should be earlier in time. I will ignore any material that post dates the middle of 1962.
NH&MRC Standards
I adopt my discussion and findings I made in the Parker judgment about the applicability of the standards.
As with Mr Parker’s matter, whether the defendant complied with or breached the standard is unknown. No testing was performed and there is no acceptable evidence as to the actual fibre count in the workplace.
Discussion on s 8(4) of the Dust Diseases Act 2005
I adopt my discussion and findings as set out in the Parker judgment. Subject to the amendment discussed, I accept and adopt the finding made by O’Meally J in Norman Wren v CSR Limited and Midalco Pty Ltd.[14] I have not had regard to those articles that were published after the middle of 1962.
[14] Dust Diseases Tribunal of NSW No 23 of 1997.
Expert Evidence/Liability
Mr Stewart and Mr Rogers gave evidence relevant to both matters. In this matter Mr Stewart, who was called for the plaintiff, purported to do a “time weighted average calculation” estimating the amount of respirable fibre to which Mr Cadoo may have been exposed. For the reasons expressed in the Parker judgment I reject the calculation.
I accepted generally Mr Stewart’s evidence when I made findings in Mr Parker’s matter (where no “calculation” was performed). I make the same findings in this matter. I rejected the evidence of Mr Rogers in Mr Parker’s matter. I generally adopt those findings here.
The report of Mr Rogers in this matter[15] is different in some respects to his report in Mr Parker’s matter. That is to be expected as he was asked to make different assumptions about the plaintiff’s work history.
[15] Exhibit DC3.
There are some minor differences between the appendices to the reports which are in my view of no consequence.
The findings I made in the Parker matter apply here. I reject the evidence of Mr Rogers generally.
I reject his evidence about trying to reconstruct a “time weighted average” from work performed over 40 years ago. I am not satisfied on the balance of probabilities that the defendant has established that Mr Cadoo’s “time weighted average” exposure of asbestos fell below the standards proposed by the NH&MRC at the time. As mentioned, I reject Mr Stewart’s evidence relating to his calculation as well.
I find that no testing was performed by the defendant. I am unable to make any findings as to the amount of fibre/dust containing asbestos to which the plaintiff was exposed.
Findings on Reasonable Foreseeability
On the evidence there clearly was a foreseeable risk of injury to the plaintiff and other employees working at the “fit-out” wharf.
As I found in the Parker matter, it was not in dispute in the literature after the 1930s that employers needed to be aware of the dangers of working with asbestos and that precautions should be taken to reduce the risk. Dust minimisation and suppression is constantly referred to as appropriate measures an employer should take. The literature did not seek to confine such matters to textile factories. As knowledge increased it became clear that any employer dealing with asbestos needed to be careful and reduce employees’ exposure to asbestos.
It is also clear from the articles that there was available from the 1930s, equipment that could be used to measure the amount of dust including asbestos that employees were exposed to in their work area.
I have accepted Mr Cadoo and the other witnesses as to the conditions under which they worked. It was a dusty environment. I find that the plaintiff worked, as found, in employment where he had regular exposure to asbestos dust while working on the PJ Adams. Indeed I accept that often there were visible levels of dust and that dust almost certainly included respirable asbestos fibre. I am unable to make a positive finding as to whether such an observation means that the amount of “dust” in the air would lead to a conclusion that the NH&MRC standards were necessarily breached. I am unable to say what the actual level of exposure to the plaintiff was. However I find that the defendant, prior to 1972 made no attempt to measure the “dust” levels at their dockyard. It, quite simply, had no idea itself of what the exposure levels were at the time Mr Cadoo was exposed. I have rejected the evidence of the attempt by Mr Rogers to “reconstruct” the level.
I find that throughout the time Mr Cadoo worked the defendant ought to have known or ought to reasonably have foreseen that:
1The use by it of asbestos products as part of its shipbuilding activities at Whyalla would release into the atmosphere respirable asbestos fibres/dust in the vicinity of their employees who were working on the ship while it was at the “fit out” wharf.
2Workers such as the plaintiff would, in the course of their work, be exposed to a level of respirable asbestos fibres/dust.
3It was established scientifically that exposure to respirable asbestos fibre could give rise to the risk of a life threatening disease or a serious debilitating disease. This risk was certainly not far fetched or fanciful.
4Such scientific material was readily available and generally in the public domain.
I find that taking all those matters into account, the fact that a risk of harm would be created or contributed to by the acts or omissions of the defendant, was reasonably foreseeable.
Breach of Duty
As discussed the inquiry at the “breach” stage involves identifying with some precision what a reasonable person would have done by way of response to the foreseeable risk.
I have to consider the magnitude of the risk and the degree of probability of it’s occurrence along with the expense, difficulty and inconvenience of taking alleviating action and any other conflicting responsibilities the defendant may have had.[16]
[16] Amaca Pty Ltd v Hannell (2007) 34 WAR 109.
The magnitude of the reasonably foreseeable risk of harm to those who undertook the work of the kind undertaken by the plaintiff over the period of time that the defendant is alleged to have breached its duty, is extremely important in relation to the question of what steps a reasonable person in the position of the defendant ought or should have taken to ameliorate the risk.
I remind myself that although the inquiry into breach is factual, a hindsight analysis is to be avoided.
It is for the plaintiff to demonstrate that there was something that the defendant could have done which would eliminate or reduce the risk complained of and which was practicable. The fact that a person ought to have foreseen a risk does not, of itself, justify a conclusion that the person was negligent in failing to take precautions against it.
I find that it was not until after 1972 that the defendant instituted any system of “dust sampling” to ascertain the level of respirable asbestos fibre in the workplace. Equipment for testing was available and indeed had been available for some time. That the defendant eventually did so is confirmed by the memo from Mr RG Hawke of 24 May 1976.[17] The terms of that memo indicate that the sampling is “new”. There is, for example, no suggestion in the memo of comparing the current reading with an earlier sample. Indeed the contrary can be inferred from the document; there was no earlier sample.
[17] Exhibit P10 page 330.
Taken in conjunction with the Wilson report, I am satisfied that no “sampling” was done until after 1972.
No witness gave evidence of seeing any dust sampling taking place.
Sampling should have been conducted. The use of asbestos related products and the fact that the work environment was “dusty” clearly called for measures to be taken.
To identify potential risks to their employees, a defendant needed to know what the components of the dust were, the concentration of the various components and the proximity of its employees to that dust. From the evidence of the plaintiff and his lay witnesses (and including the other evidence that supported it), I find that the defendant did not conduct any investigation (other than receive the government Wilson report that post dated 1962) that would have enabled them to determine appropriate measures to adopt to reduce the risk. There were means available to the defendant to sample the dust and have the samples analysed.
In one sense the magnitude of the risk is unknown as there were no samples taken. The presence of dust in the air does not of itself establish, with certainty, a particular quantity of fibre/dust being present in the air. Indeed, it was possible on the evidence I accepted from Mr Rogers that there could be an unacceptable level that was not visible to the naked eye.
The presence of the dust certainly raises the risk that there was present in the atmosphere an unacceptable level of fibre/dust. The conditions as I have found them to be indicate the potential of a risk where dust conditions were obvious to the naked eye. The presence of the dust and over the period found in my view raises the magnitude of the risk to the employees such as the plaintiff.
The defendant did not appear to take any steps before 1973 to ascertain the risk and attempt to minimise it other than chest X-rays on some workers.
Under the question of “reasonable foreseeability” I have made findings as to the state of the knowledge/literature at various times. I do not intend to repeat those matters.
I have already found that the defendant knew or ought to have known that various measures could be taken to reduce the risk of exposure. The means of reducing the risk were simple.
These were published in the scientific and medical articles as discussed. They included the minimisation of exposure by warning the workers of the dangers of asbestos exposure, by supplying the workers with respirators (masks) to use, wetting down asbestos dust to minimise the dust in the air and the use of industrial vacuum cleaners to clean up the dust.
I find that the defendant made no satisfactory attempt to minimise the dust exposure. While there was a “sweeping regime” in place this did not involve the use of industrial vacuum cleaners. The sweeping regime that was in place added to the dust in the air. The evidence was that there was no attempt by the defendant to wet down any of the asbestos dust not just at the stage of it being swept, but at any stage during these operations.
I find there was no ventilation system operating while Mr Cadoo was working. The ships did have ventilation systems installed at some stage in some areas of the ship. I have only general information about that. However, the evidence establishes that no extractor fans or ventilation system was generally operating while workers used or cleaned up asbestos.
I accept Mr Cadoo’s evidence that he was not warned by the defendant of the dangers of working with asbestos. Further, I find that the plaintiff was not warned by the defendant of the dangers of working in the areas where there was the risk of exposure to asbestos. He was not provided with the option of working with a mask or a respirator.
From all of the oral evidence called (including affidavit and other evidence) by the plaintiff, I find that the defendant provided no ventilation whilst the ships were at the “fit-out” wharf, and did not take adequate steps to suppress the amount of dust and fibre that was being generated by the trades.
As with the Parker matter, I agree with the submission of Mr Little SC that there is no evidence or no reliable evidence that the defendant took any steps to protect its workers, including the plaintiff, from the effects of cumulative asbestos exposure while he was working on the ship at the “fit-out” wharf.
Without steps to minimise the exposure the probability of harm was significantly increased. The potential problems that could arise from exposure included serious and debilitating lung disease as well as an increase in the likelihood of contracting a life threatening illness.
The magnitude of the risk has to be looked at in the context of the difficulty in minimising it. It would not have been an expensive or difficult task to put in place those matters mentioned above. Subsequently they were the recommendations of Dr Wilson in 1968.
I reject the submission by the defendant that such matters were simply a matter of “good housekeeping”. Steps were required to minimise the risk of injury. Mr Cadoo was employed in an area where precautions, which had been recommended in the literature over many years, were simply not taken.
I find that the defendant breached its duty of care in that it:
(a) Did not warn workers exposed to asbestos dust and fibre of the dangers of asbestos dust and fibre.
(b) Did not provide masks or respirators to workers exposed to asbestos dust and fibre.
(c) Did not require workers exposed to asbestos dust and fibre to wear a mask or respirator.
(d) Did not reduce the amount of airborne dust on board ships at the “fit-out” wharf by using extractor fans or wetting down dust or ensuring that dust was cleaned up regularly by use of industrial vacuum cleaners.
(e) Did not instruct workers on how to avoid exposure to asbestos dust and fibre.
I therefore find the defendant liable in negligence.
Breach of Contract
It was agreed that there was an implied term in the contract of employment that the defendant would take reasonable care for the plaintiff’s health and safety. The content of the terms co-exist with the defendant’s obligations in negligence. My findings on the negligence cause of action are therefore relevant to the breach of contract claim.
Given my findings, it is unnecessary for me to consider the question of “nominal” damages.
Statutory Duty
Given my findings in relation to the question of negligence, it is not necessary for me to discuss the breach of statutory duty claim.
Medical Evidence
On general matters I adopt the findings in the Parker judgment.
In this matter the plaintiff called Professor Ruffin to give evidence as well as Dr Sally Chapman. There was no dispute about their qualifications. Professor Alpers’ reports were tendered.[18]
[18] Exhibits P14A, P14B, P14C, P14D.
Dr Antic gave evidence for the defendant. His qualifications were not challenged. In so far as is necessary about general medical matters, I accept the evidence of Professor Ruffin as discussed in the judgment of Parker.
Dr Chapman examined Mr Cadoo at the request of his general practitioner for evaluation of “increased cough and breathlessness”.[19] She saw him in her rooms on several occasions and Mr Cadoo was admitted to hospital for a short period of time in February 2000. Dr Chapman took a history from him that included an occupational history: she also arranged lung function testing as well as radiological examinations.[20]
[19] T 309.
[20] T 309.
When Dr Chapman initially spoke to Mr Cadoo he made no mention of any exposure to asbestos. Dr Chapman said that it was part of her usual practice to ask such a question. Mr Cadoo made mention of his welding.
I find it is likely that Dr Chapman did ask that question. Why Mr Cadoo made no mention of any exposure to asbestos remains a mystery. He clearly did have exposure to asbestos in England and Australia. It was not suggested by the defendant that he had no exposure to asbestos.
The relevance of the failure of Mr Cadoo to mention his exposure to asbestos lies in the initial diagnosis made by Dr Chapman.
Two reports of Dr Chapman were tendered, one dated 5 November 2001 and the second dated 11 March 2009.[21] Her initial opinion was that Mr Cadoo had “idiopathic pulmonary fibrosis”. Idiopathic simply referred to an unidentified cause. Dr Chapman based the diagnosis on the findings of a restrictive ventilatory defect on lung function, fibrosis on a CT scan and an absence of other known cause of interstitial lung disease”.[22]
[21] Exhibit PC4, Exhibit PC4A.
[22] Exhibit PC4 page 3.
By the time the report was written Dr Chapman was aware of the exposure to “asbestos dust and fibre”. At that time a CT scan did not show evidence of a “pleural plaque”. In the report she stated if Mr Cadoo “has a documented significant exposure to asbestos then his interstitial lung disease may be due to asbestos …”
In her report of 11 March 2009, Dr Chapman stated:
On the balance of probabilities I believe that the late Mr Cadoo was suffering from asbestosis. I base this on the findings of a restrictive ventilatory defect on lung function, fibrosis on CT scan and his Affidavit detailing asbestos exposure.[23]
[23] Exhibit PC4A page 2.
When Dr Chapman gave evidence she was shown a CT scan of 20 February 2003.[24] This scan had not previously been available for inspection.
[24] Exhibit PC3.
Having inspected the scans Dr Chapman stated:[25]
The CT scans from 2003 show evidence of interstitial lung disease with anteroseptal thickening, degree of honeycombing, particularly at the bases. Both of those features, although at an earlier stage were seen, when I saw him – on the CT scans in 1999; however, on the 2003 scans, there is significant pleural thickening which was not evident on the previous scans, and there’s also an area of pleural calcification, which would be consistent with a pleural plaque, and one of the common causes of pleural plaques is asbestos exposure. So, by having a history of worked as a welder with those signs, with additional radiological signs, would make me suspect that there was an underlying cause for his pulmonary fibrosis, which was exposure to asbestos.
[25] T 313.
Dr Chapman said that the “pleural changes” are a marker of asbestos exposure and in most circumstances, don’t impact on the function of the lungs.[26]
[26] T 330.
Regarding her original diagnosis of “idiopathic pulmonary disease” Dr Chapman stated:[27]
[27] T 331.
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QBut you would agree with me, wouldn’t you, that it’s equally possible that you could have pleural changes caused by asbestos exposure and you could have fibrotic change in the lung caused by something else.
AYou could. But – in general with interstitial lung disease you would only call it idiopathic in the absence of any other plausible explanation. That’s the definition of idiopathic pulmonary fibrosis from a medical perspective; pulmonary fibrosis without a known cause for it.
QIt’s not a known cause. Are you saying without a plausible other cause.
AWithout a plausible other cause, yes. So certainly you can – it’s very difficult to say that they couldn’t occur independently but, if you are saying that idiopathic pulmonary fibrosis by definition is pulmonary fibrosis without another explanation, if you have another explanation it’s no longer idiopathic.
QIs what you are saying as soon as one identifies a plausible other cause one departs from the diagnosis of idiopathic pulmonary fibrosis.
AYes.
QAnd one adopts asbestosis.
AWell, asbestosis or autoimmune related or whatever.
QIf it’s silica you would say silicosis.
AYes.
QAnd that’s the basis on which you’ve diagnosed asbestosis.
AYes.
QNamely plausibility based on what you’ve been told.
AYes.
HIS HONOUR
QAnd seen.
ASeen the supporting evidence of the pleural plaque.
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QNot based on any particular satisfaction on the array of causes that actually is the one.
AAs part of the efficient valuation of pulmonary fibrosis other causes are looked, at particularly autoimmune markers, and his were all negative in 1999. Apart from that generally the diagnosis of pulmonary fibrosis, you would not necessarily go searching for another cause.
QYou haven’t gone searching or investigating all other potential causes.
ANo.
QYour approach has been seen ‘As soon as I am shown something which plausibly indicates asbestosis then it’s asbestosis’.
AYes.
Professor Ruffin was also called to give evidence. Two reports prepared by him were tendered.[28]
[28] Exhibit PC1, Exhibit PC2.
Professor Ruffin initially saw Mr Cadoo in early 2002. He took a history from Mr Cadoo which included the fact of exposure to asbestos at various times during Mr Cadoo’s working life.
No finger clubbing was noted. Basal bilateral respiratory crackles were heard on testing. Scans taken on 18 October 1999 and 2 August 2000 showed “pleural thickening and basal fibrosis. Chest X-rays showed basal interstitial changes.
Professor Ruffin diagnosed Mr Cadoo as suffering “pleural thickening together with a mild degree of asbestosis”. He thought Mr Cadoo’s previous asbestos exposure to be the likely cause of his pleural thickening and basal fibrosis. He noted there is existing cardiovascular disease and thought that this condition was “the limiting factor in his life”.
In his report of 28 April 2009, Professor Ruffin, having received a report of 20 February 2003 scan, in addition to a post mortem report and lung function tests, confirmed his earlier diagnosis.
When Professor Ruffin gave evidence he had access to the actual scans taken on 2 February 2003.[29] He noted “some calcification adjacent to the pleura in the mediastinal settings at window 120 mm”.[30] He had not commented on that previously. Professor Ruffin thought the scans were supportive of his diagnosis, particularly the previously unnoticed calcification.[31]
[29] Exhibit PC3.
[30] T 130 line 21.
[31] T 131 line 31.
Professor Ruffin’s evidence is consistent with that of Dr Chapman.
As mentioned, the plaintiff also tendered the reports of Professor Alpers (now deceased). In general terms his diagnosis was consistent with the final opinions of both Dr Chapman and Professor Ruffin.
Dr Antic gave evidence for the defendant. His reports of 12 September 2008 and 15 December 2008 were tendered.[32]
[32] Exhibits DC2, DC2A.
Dr Antic, in his initial report, accepted that Mr Cadoo had interstitial disease complicated by fibrosis. He questioned however, the link in this case between the asbestos exposure and interstitial lung disease.[33]
[33] Exhibit DC2 page 2.
When Dr Antic gave evidence, he had access to the scans Exhibit PC3. In relation to the observation about a “pleural plaque” he said:
He was not sure about that, it may be a pleural plaque within a fissure between two lobes of the lungs. It’s not a pleural plaque seen in the normal place … It could equally be an old scar from an old infection such as tuberculosis and so one is left uncertain …[34]
[34] T 644 line 4.
He used “teaching scans”[35] to demonstrate his position.
[35] Exhibit D4.
He said initially that he “was uncertain as to whether the problem is asbestosis or not”.[36]
[36] T 643.
Dr Antic said that an “old” TB scar could have been missed on previous CT scans.[37]
[37] T 682.
When cross-examined, Dr Antic said:
AYes, but to cut to the chase, the issue that I put previously to your Honour was that the thing that made me as Dr Chapman think twice, was the presence of upper zone abnormalities rather than purely basal abnormalities as one sees in the evolution of pulmonary asbestosis. That is the main decision maker in this case, now I’m comfortable in the presence of pleural thickening and the asbestos exposure, to seriously consider the possibility that this is pulmonary asbestosis. One has to do that, because that’s what the rules are, but there are these unusual features which I wanted to – and Dr Chapman brought to the attention of everybody.
However, while maintaining that the diagnosis was not obvious he said:
QAnd interstitial fibrosis, more probably than not, as a result of asbestos exposure, you’d agree with that wouldn’t you.
AI think on the balance I should agree with that, with all the qualifications that I’ve made about it before, but I think on the balance of probabilities in the presence of pleural thickening and the exposure one has to concede that that is the more likely explanation.
The concession by Dr Antic was in my opinion properly made. The evidence pointing to asbestosis as the diagnosis, on the balance of probabilities, was compelling.
I accept the evidence of Dr Chapman and Professor Ruffin. While I do not have to rely on the concession made by Dr Antic it was properly made on the evidence now adduced.
I find, on balance, that Mr Cadoo at the time of his death was suffering from both asbestosis and asbestos related pleural disease. These conditions were present as early, at least, as 1999.
It was common ground that these conditions did not contribute to his death.
Causation
I have found that Mr Cadoo suffers from a “dust disease”. I adopt the findings in relation to the question of causation from the Parker judgment.[38]
[38] Parker v BHP Billiton Limited [2011] SADC 104 at [851]-[858].
Degree of Impairment and Damages
An affidavit of Mrs Cadoo dated 24 January 2009 was tendered.[39] It was a “Statement of Loss”.
[39] Exhibit PC16.
The following matters are established from the affidavit.
Mr Cadoo became ill in 1998 with a respiratory illness during which he developed a cough and a wheeze. He saw his general practitioner who prescribed Prednisolone and antibiotics. He suffered a similar illness in June 1999. He again was prescribed Prednisolone.
From late 1999 Mr Cadoo suffered shortness of breath which quickly became worse. He was referred to a specialist and underwent various tests. In early 2000, Mr Cadoo was admitted to the Burnside Hospital and later St Andrews Hospital for a total of approximately three weeks. Mrs Cadoo stated that it was about this time that Mr Cadoo’s activities became curtailed. By 2002 he was unable to do very much at all.
In April 2003 his condition rapidly deteriorated and he died on 17 April 2003.
While not putting a specific time frame on matters, Mrs Cadoo stated that as a result of his breathlessness and lethargy Mr Cadoo frequently felt unwell and was largely housebound. She assisted him to shower, toilet and dress as well as getting him into bed. Mr Cadoo was unable to look after the gardening, lawn mowing, shopping, driving and other household tasks.
Mr Cadoo in his affidavit[40] signed on 17 June 2002 does not discuss those issues. The affidavit discussed his work history and exposure to asbestos. He mentions that over “the last couple of years my health has deteriorated significantly. I find that I am increasingly short of breath”.
[40] Exhibit PC5.
This is consistent with Mrs Cadoo’s affidavit.
It was common ground between the medical experts that Mr Cadoo suffered from other medical problems including a heart condition. This condition ultimately led to his death.
Between the experts there was also consistency about the contribution the condition of asbestosis made to his overall disability.
Professor Ruffin saw Mr Cadoo in early 2002. He noted that Mr Cadoo had a problem with “exertional dyspnoea over the past two and a half years”. He further noted that Mr Cadoo walked with a stick because of “weakness in his legs”. His walking distance on the flat was “about 50 metres”. Professor Ruffin noted that he was “able to shower himself but is unable to help with household chores because of dyspnoea”. He noted that he was a “frail looking man”. Mr Cadoo had been a “smoker”.
Professor Ruffin in his report of 28 April 2009, having assessed a number of lung function tests, stated:
On balance I think that the major impact of disease on his lung function tests is related to his restrictive problem for which interstitial disease from asbestosis in the likely cause.
He further stated:
… the inability to undertake activity such as carrying heavy objects, climbing hills or prolonged mowing of the lawn would have been the consequence of his disease status based on the lung function tests in 2002. Hence he may have required assistance in performing tasks around the house such as mowing lawns or having to climb ladders or carry heavy objects.
Professor Ruffin was challenged in cross-examination about his diagnosis. I have already dealt with that aspect.
Dr Chapman first saw Mr Cadoo on 29 September 1999. At that time he did not report significant dyspnoea. On 27 October 1999 he reported exertional dyspnoea and this had worsened such that by 17 November 2009 he had dyspnoea on minimal exertion.
He was prescribed Prednisolone which improved his symptoms but he suffered “side effects” from the medication.
In her report of 11 March 2009, Dr Chapman stated: “I last saw Mr Cadoo in March 2000. At that time he did not require care and assistance in his daily activities.” She was unable to comment on his “care” requirements after that time.
Dr Chapman gave the following evidence when cross-examined.
QYou’ve now told us that, as you now reinterpret what was going on in the six months that you were looking after Mr Cadoo, that he had I think a disease you referred to as alveolitis possibly consequent upon some viral episode.
AYes.
QWhich was to some extent masking the fibrosis that was there as well.
AThat’s what I believe.
QThe fibrosis on its own at that time wasn’t having any impact on his lung function, was it.
AHe had reduced lung function which was probably a combination of the underlying pulmonary fibrosis, the more acute alveolitis and possibly from a degree of congested cardiac failure.
QEven as early as 2000.
AYes.
QDid you find that he was affected by cardiac failure in 2000.
AYes, I did.
QOf those three factors, the underlying fibrosis was the least significant in terms of impact on his lung function; true.
AI don’t think that it’s possible to quantify – to make that sort of statement. From the alveolitis point of view he would have been at his best when he was on the highest dose of Prednisolone. I just was to clarify when that was. On 15 December 1999 his lung function testing still showed a moderate restrictive defect with lung capacity of 70% of predicted and functional capacity – diffusing capacity, which is the transfer of gas from air to the lungs of around 63%.
QWhat are the possible causes of that defect as they were at that time.
AAt that stage he was on high dose treatment for the alveolitis so I think the effect of the alveolitis would be minimal at that stage. There was no evidence in my notes of him having a congested cardiac failure so I would suggest that the lung function on 15 December 1999 would be reflective of his underlying fibrotic lung disease. (My underlining)
QWould you agree with the characterisation of his fibrotic disease at that stage of being mild.
AYes.
QIs it possible that at that stage that mild fibrotic disease, taken on its own, was having no practical effect on his breathing.
AAt that stage he reported being mildly short of breath on walking uphill. So the degree of impact on his life was that it was not having an impact on daily activity. It was having an impact on greater than usual exertion.
QIs it possible that the impact from greater than usual exertion would have been there having regard to the other factors that were affecting him, even if he had no fibrosis.
ACertainly his cardiac failure may have contributed – cardiac dysfunction may have contributed to exertion at that stage. I don’t think the alveolitis would have been a factor at that point.
QBut any disability that he was suffering on exertion might have been attributable solely to his cardiac failure.
AIt’s possible.
QOn the information available to you you wouldn’t be able to make any other comment than that.
ANo.
QAnd if he later reported breathlessness, that is in 2002 or 2003, that again might be the product of cardiac failure alone; correct.
AIt’s possible.
QOr it might have been the product of cardiac failure assisted to a mild degree or contributed to by a mild degree also with his fibrotic condition.
AYes.
QAnd it wouldn’t be possible on the information available to you to make any sensible determination between those two possibilities.
ANo, that’s not something I could do.
Professor Alpers saw Mr Cadoo on 4 April 2002.[41] He noted:
His general health is not good. He gets very short of breath, it is particularly worse in the last two years. His exercise tolerance is about 10-20 yards, he can’t climb stairs or do much around the house at all and gave up lawn bowls a few years ago.
[41] Exhibit PC14A.
Professor Alpers noted that he had a “quite marked restriction, loss of diffusing capacity and reduced spirometry, overall a 35% lung function deficit.”
Professor Alpers saw him again on 20 February 2003.[42] He noted:
Since I saw him last he says his breathing is much worse and he is now having difficulty even dressing and his wife has to help him. He is able to walk about 20m with a walking frame.
[42] Exhibit PC14B.
Dr Antic did not have the opportunity to examine Mr Cadoo.
In his reports Dr Antic was not prepared to accept the diagnosis that the pulmonary fibrosis was necessarily connected to asbestos exposure. He did however accept that Mr Cadoo’s lung disease contributed about 30 per cent to his disability.
As mentioned, Dr Antic conceded when he gave evidence that, given the further information, Mr Cadoo on balance suffered from asbestosis.
In relation to the contribution the fibrotic changes made to his condition, Dr Antic said:
QAnd if you were asked to assume that he had complained of breathlessness in the months leading up to the time when these scans were taken, would it be your opinion that the breathlessness was likely attributable to asbestosis – sorry to the fibrotic change in his lung or to the heart difficulty, which you’ve said he had.
AWell it is likely that both made a contribution and it’s likely that the heart failure made a very significant contribution to the breathlessness.
QAre you able to put any – are you able to say with any precision as to whether the fibrotic changes would have had any impact during that period or not.
AThey would have had some impact.
QAre you able to put any quantification on that.
ALook it’s very difficult and I would have taken some note of the level of breathlessness that preceded in the previous years to try to work out a percentage and I would of – and this is by no means a good estimate, but I would expect that something like 30-40% of the breathlessness to have been caused by the fibrotic change.
Generally speaking, Mrs Cadoo’s affidavit is consistent with the observations of the medical witnesses. I take into account it was prepared for the purpose of litigation and not subject to cross-examination. I accept her evidence.
I find that his asbestosis condition was of a progressive nature. The disability he had when seen by Dr Chapman in early 2000 was not particularly debilitating. Shortly before his death his condition related to asbestosis had deteriorated. Clearly he had other serious problems as his death related to his cardiac condition not asbestosis.
Professor Ruffin saw him in 2002 after Mr Cadoo’s condition had progressed. He thought, as already discussed, that “the major impact of disease on his lung function tests is related to his restrictive problem for which interstitial disease from asbestos is the likely cause”.
Dr Antic was asked a more general question – not one related to 2002. He considered 30-40 per cent of his breathlessness could be ascribed to fibrosis. Dr Antic considered that to be a “broad estimate”. Whether Dr Antic would have conceded that degree of contribution from early 2001 is not entirely clear.
Dr Chapman would not give an opinion. She did state however that, due to the Prednisolone treatment in 1999 the affect of his alveolitis would have been minimal in 1999. Cardiac dysfunction may have been contributing to the problem. Professor Alpers, like Professor Ruffin, only saw Mr Cadoo in 2002.
As mentioned, there is general consistency between the medical opinions depending on the time of the assessment.
I accept Dr Antic’s “broad assessment” of a 30-40 per cent contribution. I will adopt the lower end of his assessment in the circumstances.
I do not accept the defendant’s submission that Mr Cadoo asserts a “gradually increasing breathlessness starting in 2002”. Mr Cadoo stated: “Over the last couple of years my health has deteriorated significantly. I find that I am increasingly short of breath”.
His affidavit is dated 17 June 2002. Clearly he is asserting an earlier onset of his breathlessness. That is consistent with the affidavit of Mrs Cadoo and the medical reports.
Mr Cadoo’s breathlessness was evident in 1999 but was not a significant problem.
I find that his breathlessness became a significant problem around early 2001, it then progressed. As Mrs Cadoo stated, and I accept, by “early 2002 he was unable to do very much at all.”
In their submissions, both parties relied on “costings” tendered in Mr Parker’s matter. That position is in line with the understanding reached at the beginning of the matters as to the question of cross admissibility between the actions. What differed between the two actions was the assessment of the disability and the number of hours of assistance required, not the cost of providing the assistance (to any significant degree).
For the period of 1 July 2001 to 30 June 2002, I find Mr Cadoo would have required about eight hours per week of assistance. The eight hours includes assistance cleaning the house, meal preparation, assistance in shopping as well as some assistance in helping to wash, dress and groom. I cannot be precise about the cost but taking into account the evidence on costing[43] I allow $25 per hour.
8 hours per week @ $25 per hour = $200 per week
52 weeks = $10,400[43] Exhibits P15A, P15B, D15.
From 30 June 2002 to 8 April 2003, Mr Cadoo’s needs would have increased significantly.
There is very little evidence as to a time frame or precisely what care would be required. However, mere difficulty in estimating damages does not relieve a court from the responsibility of estimating them as best it can.
The defendant submitted that an allowance of $360 per week would be generous. In the latter stages of his life the amount of care required would have significantly exceeded a cost of $360 per week. I accept that the defendant was suggesting that amount over the 40 week period as an average. However, the evidence is clear that by mid 2002, Mr Cadoo’s condition had deteriorated significantly. The cost of nursing care was obviously higher than cleaning services[44].
[44] Exhibits P15A, P15B.
Taking all those matters into account, I allow $500 per week for this period of time.
40 weeks @ $500 per week = $20,000
Payments made by the Health Insurance Commission were agreed at $2,896.00. Whether they related in any way to his compensable condition was not agreed.
I accept the defendant’s submission that in part at least, some of the early attendances related at least solely to the “alveolitis” described by Dr Chapman. What her opinion was of the contribution of the asbestos related illness at that time (given her later views after the further history and later scans) is not clear.
To take those matters into account, I will not allow the full amount pursuant to the Health Insurance Commission notice. I allow $2000.
I allow half of the plaintiff’s claim for lawn mowing (as it was not required from 1999).
Taking into account the fact that the condition was progressive, I find that overall that 30 per cent of the disability related to his compensable injuries.
Out of Pocket Expenses
$ Lawn Mowing 30% of $627.69 188.30 HIC (no deduction) 2,000.00 Past Gratuitous Services ($)
10,400
20,000
30% of 30,400
9,120.00
Interest on Gratuitous Services
(claimed at 4%)
4,000.00 Total $15,308.30
The parties agreed that six per cent of the damages were attributable to his exposure at Whyalla.
6% of $15,308.30 = $918.50
I therefore assess damages at $918.50.
The defendant raised in submissions the rule against “double satisfaction” in relation to this matter. I will hear the parties further on this aspect given my findings in relation to this matter and Mr Parker’s claim.
I will hear the parties as to the form of the order and costs.
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